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Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or BakA novel BH3 ligand that selectively targets Mcl-1 reveals that apoptosis can proceed without Mcl-1 degradationProapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunityGene structure alternative splicing, and chromosomal localization of pro-apoptotic Bcl-2 relative BimBH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytesInduction of BIM, a proapoptotic BH3-only BCL-2 family member, is critical for neuronal apoptosisCharacterization of a premeiotic germ cell-specific cytoplasmic protein encoded by Stra8, a novel retinoic acid-responsive geneBIM regulates apoptosis during mammary ductal morphogenesis, and its absence reveals alternative cell death mechanismsConcomitant loss of proapoptotic BH3-only Bcl-2 antagonists Bik and Bim arrests spermatogenesisLoss of PKD1 and loss of Bcl-2 elicit polycystic kidney disease through distinct mechanismsCombined loss of proapoptotic genes Bak or Bax with Bim synergizes to cause defects in hematopoiesis and in thymocyte apoptosisDegenerative disorders caused by Bcl-2 deficiency prevented by loss of its BH3-only antagonist BimPolycystic kidney disease prevented by transgenic RNA interferenceER stress triggers apoptosis by activating BH3-only protein BimFas-mediated neutrophil apoptosis is accelerated by Bid, Bak, and Bax and inhibited by Bcl-2 and Mcl-1Anti-apoptotic gene Bcl2 is required for stapes development and hearingBoth leukaemic and normal peripheral B lymphoid cells are highly sensitive to the selective pharmacological inhibition of prosurvival Bcl-2 with ABT-199.BCL-2 is dispensable for thrombopoiesis and platelet survivalGlucose induces pancreatic islet cell apoptosis that requires the BH3-only proteins Bim and Puma and multi-BH domain protein Bax.Shutdown of an acute T cell immune response to viral infection is mediated by the proapoptotic Bcl-2 homology 3-only protein Bim.Negative selection of semimature CD4(+)8(-)HSA+ thymocytes requires the BH3-only protein Bim but is independent of death receptor signaling.Type I interferon drives dendritic cell apoptosis via multiple BH3-only proteins following activation by PolyIC in vivo.Reexpression of retinoic acid receptor (RAR) gamma or overexpression of RAR alpha or RAR beta in RAR gamma-null F9 cells reveals a partial functional redundancy between the three RAR types.Antiapoptotic Mcl-1 is critical for the survival and niche-filling capacity of Foxp3⁺ regulatory T cellsFatal hepatitis mediated by tumor necrosis factor TNFalpha requires caspase-8 and involves the BH3-only proteins Bid and Bim.Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome.Control of apoptosis in hematopoietic cells by the Bcl-2 family of proteins.Individual and overlapping roles of BH3-only proteins Bim and Bad in apoptosis of lymphocytes and platelets and in suppression of thymic lymphoma developmentXIAP discriminates between type I and type II FAS-induced apoptosis.BCL-2 family member BOK is widely expressed but its loss has only minimal impact in mice.NKT cell stimulation with glycolipid antigen in vivo: costimulation-dependent expansion, Bim-dependent contraction, and hyporesponsiveness to further antigenic challenge.Mcl-1 is essential for germinal center formation and B cell memoryElevated Mcl-1 perturbs lymphopoiesis, promotes transformation of hematopoietic stem/progenitor cells, and enhances drug resistance.Pro-apoptotic BIM is an essential initiator of physiological endothelial cell death independent of regulation by FOXO3.BH3-only proteins - evolutionarily conserved proapoptotic Bcl-2 family members essential for initiating programmed cell death.The RUNX3 tumor suppressor upregulates Bim in gastric epithelial cells undergoing transforming growth factor beta-induced apoptosis.Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic.Destruction of tumor vasculature and abated tumor growth upon VEGF blockade is driven by proapoptotic protein Bim in endothelial cells.The control of apoptosis in lymphocyte selection.Defects in the Bcl-2-regulated apoptotic pathway lead to preferential increase of CD25 low Foxp3+ anergic CD4+ T cells.
P50
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P50
description
hulumtues
@sq
researcher
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wetenschapper
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հետազոտող
@hy
name
Philippe Bouillet
@ast
Philippe Bouillet
@en
Philippe Bouillet
@es
Philippe Bouillet
@nl
Philippe Bouillet
@sl
type
label
Philippe Bouillet
@ast
Philippe Bouillet
@en
Philippe Bouillet
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Philippe Bouillet
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Philippe Bouillet
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altLabel
Bouillet P
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prefLabel
Philippe Bouillet
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Philippe Bouillet
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Philippe Bouillet
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Philippe Bouillet
@nl
Philippe Bouillet
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P1053
E-1241-2013
P106
P21
P31
P3829
P496
0000-0002-9012-6058